Conditions Flashcards

1
Q

What is the definition of a collapse?

A

A collapse is a sudden transient loss of consciousness leading to a fall.

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2
Q

What are the two main types of collapse?

A

Syncope & Non-syncopal attacks

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3
Q

What is syncope? What is the pathophysiology?

A

Syncope is sudden, transient & self limiting loss of consciousness caused by transient global cerebral hypoperfusion

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4
Q

What are the main causes of syncope? (4)

A

Acute illnesses
infection, dehydration, MI, PE, Haemorrhage, Aortic dissection

Neurally mediated reflexes

  • Vasovagal syncope (faint)- vagal stimulation secondary to a stimulus ( e.g. pain, fright, emotion) —> reflex bradycardia & vasodilation —> hypotension —> syncope, usually an autonomic prodrome ( pale, clammy, light-headed), followed by nausea/abdo pain —> syncope

-Situational syncope
reflex mediated via Vasovagal system, but to specific stimuli
E.g. cough/sneeze, defecation, post exercise, long periods of strain

-Carotid sinus hypersensitivity
- increased pressure ( e.g. neck turning) on hypersensitive carotid body ( baroreceptor)—> bradycardia & vasodilation —>hypotension —> syncope ( common in elderly)

Orthostatic

  • Orthostatic (Postural) Hypotension
    Impaired autonomic reflexes —> pooling of blood in veins of lower limbs —> cerebral hypoperfusion & syncope
    Can be caused by primary autonomic failure syndromes ( within nervous system) or secondary (caused by another disease)
    Secondary - diabetes, Parkinson’s

-Medication/ Alcohol

-Volume depletion

**Cardiac related **

-Arrhythmias
Reduce cardiac output —> cerebral hypoperfusion —> syncope
Examples:
- Sick sinus syndrome
- AV blocks
- Paroxysmal SVT/ VT
- Long QT interval
- AF

-Structural
Structural deformity —> impaired ability to increase CO —> cerebral hypoperfusion —> syncope
- Aortic outflow obstruction - e.g. aortic stenosis
- Pericardial tamponade
- Hypertrophic obstructive cardiomyopathy

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5
Q

What are the causes of non-syncopal collapses/ attacks?

A

Collapse not caused by cerebral hypoperfusion:

Seizures

**Hypoglycaemia **

Intoxication

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6
Q

What are the P’s in the history of a Vasovagal syncope?

A

Position - upright
Predisposing factors - warm environment, prolonged standing
Precipitating factors - unpleasant stimuli, concurrent illness
Prodrome - pale, clammy, light-headed

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7
Q

Different presentation of syncope vs non-syncopal attacks?
- Risk factors
- Situation
- Onset
- During event
- After event
- Tests

A

Syncope

- Risk factors
PMHx - heart disease, infection, cardioactiev drugs ( thiazides & anti-arrhythmic’s)

*- Situation *
Predisposing factors - warm environment, prolonged standing
Precipitating factors - unpleasant stimuli, concurrent illness, chest pain, neck movements

*- Onset *
Prodrome - pale, sweaty, nauseous - Vasovagal
Chest pain, palpitations - dysarhythmia/ MI

*- During event *
Weak carotid pulse, low muscles tone, may have some limb jerking

- After event
Few mins for recovery
Brief period of confusion may occur
May be prolonged ( hours) of fatigue
Tongue biting & incontinence possible

- Tests
ECG - abnormal in cardiac causes
BP - orthostatic

Non-syncopal attacks/collapse

-Risk factors
PMHx - stroke, advanced dementia, seizures
Electrolyte disturbance

*- Situation * - N/A

*- Onset *
Aura may occur - gustatory / olfactory

- During event
Muscle tone may be raised with or without movement
Muscle activity and movement can also be seen
Tongue biting - common
Incontinence is comomone

- After event
Slow recovery to full consciousness with prolonged confusion ( minutes to hours)
Ictal period

*- Tests *
EEG - abnormal in seizures
CT - can be abnormal

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8
Q

What is the definition of constipation?

A

Condition in which there is delayed alimentary tract transit time, leading to:

  • the time between bowel evacuations is longer than normal for the patient
  • the stool is harder than normal
  • the total faecal mass inside the abdomen is increased
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9
Q

What are the three main types of constipation?

A

1) Hard stool impaction - hard faeces present in the rectum ( often ++)
2) Soft stool impaction - the whole distal bowel is loaded with soft putty like faeces that cannot be evacuated
3) High proximal impaction - may be due to obstructing pathology ( e.g. carcinoma)

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10
Q

What are the causes of constipation? (5)

A

1) Reduced bowel motility
- drug induced - anti-muscarinics, opiates, iron, antidepressants, antipsychotics, CCBs
- immobility
- illness
- poor diet - low fibre / dehydration

2) Failure to evacuate bowels fully
- Anorectal disease - anal or colorectal cancer, fissures, strictures, herpes, rectal prolapse, levator ani syndrome
- reduced toilet access
- lack of privacy / altered daily routine ( hospital)

3) Neuromuscular - slow transit from decreased peristalsis
- Parkinson’s disease
- diabetic neuropathy pseudo obstruction
- spinal or pelvic nerve injury

4) Mechanical obstruction of the bowel
- carcinoma of the colon
- diverticular disease
-strictures

5) Metabolic / endocrine
- hypercalcaemia
- hypothyroidism
- hypokalaemia
- porphyria
- lead poisoning

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11
Q

What investigations / examinations should be considered in constipation ?

A

Per rectal examination - to check faecal incontinence and the rectum, the prostate, anal tone and sensation should all be assessed as well as a visual inspection around the anus.

Stool type should be assessed if in the rectum.

Bladder scan - check for retention

Abdominal examination - to check for obstruction / tenderness( only felt if significantly loaded)

If patient is large - may require an AXR to visualise loading if unable to feel on abdominal examination

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12
Q

What medications can be used in constipation? ( 4)

A

1) Bulking agents
- increase faecal mass - stimulate peristalsis
- Bran powder, Ispaghula husk, Methycellulose, Sterculia

2) Stimulant laxatives
- increase intestinal motility
- Bisacodyl, Senna, Docusate sodium, Glycerol suppositories

3) Stool softeners
- used in hard stool impaction - soften stool to aid evacuation
- Arachis oil (peanuts!)

4) Osmotic laxatives
- retains fluid in the bowel, stimulate peristalsis/ diarrhoea
- Lactulose - produces osmotic diarrhoea
- Macrogol (Movicol)

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13
Q

What medications do you use in soft & hard stool compaction?
What other advice could be given?

A

Soft stool faecal impaction - microlax enema, stimulant laxatives ( e.g. senna , bisacodyl)

Hard stool faecal impaction - eicosanoid enema ( aka arachis oil - oil-retention enema ) with manual evacuation - ask for peanut allergy as peanut based oil, Bulk forming laxatives (ispaghula husk & sterculia - also acts as a faecal softener)

Use lactulose in both

Non-pharmacological - regular exercise, improving access to the toilet, adequate fibre, adequate water

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14
Q

What is urinary incontinence?

A

Any involuntary leakage of urine

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15
Q

What are the main types of urinary incontinence?

A

Overactive bladder

Stress incontinence

Urgency incontinence

Overflow incontinence

Functional incontinence

Mixed incontinence

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16
Q

Define the common types of incontinence …

-Overactive bladder
-Stress incontinence
-Urgency incontinence
-Overflow incontinence
-Functional incontinence
-Mixed incontinence

A

Overactive Bladder - can be diagnosed both symptoms based & via urodynamic analysis ( detrusor overactivity) - spontaneous contractions of detrusor leads to urgency and frequency symptoms

Stress incontinence - small volumes leak during coughing/laughing( increases in abdominal pressure) –most commonly in women due to pelvic muscle and ligament laxity

Urgency incontinence - Frequent voiding, often cannot hold urine. Nocturnal incontinence is common. Commonly seen with detrusor overactivity but can occur in obstruction.

Overflow incontinence - Due to urinary retention. Seen with obstructive symptoms in men with enlarged prostates.

Functional incontinence - Often due to cognitive impairment or behavioural problems.

Mixed incontinence - mixture of both urge incontinence symptoms and stress incontinence
Vesicovaginal fistulae - occur in pelvic malignancies - leads to constant wetness

17
Q

What patient factors may influence / cause continence? (4)

A

1) Age related changes
Diminished total bladder capacity but increased residual volume
Diminished bladder contractile function
Increased frequency of uninhibited bladder contractions
Reduced ability to postpone voiding

2) Co morbidity
Increased constipation, diminished mobility ( functional incontinence)
prescribed meds affect lower urinary tract (alpha blockers) conscious state ( e.g. sedatives ) or ability to get to toilet (antihypertensives —> postural drop)
Impaired cognition ( dementia & confusion)

3) Reversible factors
UTI, Delirium
Drugs ( diuretics —> polyuria, anti cholinergics —> retention), Constipation
Polyuria ( poorly controlled diabetes, hypercalcaemia )
Uterine prolapse, bladder stones / tumours, atrophic vaginitis

4) Irreversible but treatable conditions
Pelvic floor damage & urethral musculature weakening - women, childbirth etc
Menopause - vaginal atrophy —> incontinence
Weakened Detrusor muscle
Prostate - Hypertrophy or cancer - outflow obstruction
Neurological dysfunction ( Micturition centre)
Functional incontinence - unable to make it to toilet

18
Q

How is urinary incontinence investigated?

A

Urine dipstick - UTI?, haematuria, proteinuria, glucosuria
Non invasive urodynamics. - frequency - volume chart, bladder scan - post micturition residual volume , retention?

Can do:
Invasive Urodynamics
Pad tests
Cytoscopy

19
Q

How is urinary incontinence managed?
( Non pharmacological, Medical, Surgical & interventions)

A

Non pharmacological :

Modify fluid intake
Weight loss
Stop smoking
Decrease caffeine intake (UUI)
Timed voiding
Regular toileting
Bladder retraining
Pelvic floor training

In OAB :

Anti muscarinics- monitor carefully may precipitate urinary retention
- Tolterodine 2mg bd / 4mg do
- Solifenacin 5-10 mg od
- Trospium chloride 20mg bd
- Mirabegron
- Oxybutynin 2.5 mg - 5mg tds ( be careful in prescribing in frail older people, may cause acute delirium / chronic confusion

Side effects - dry mouth ( xerostomia, constipation)
Titration dose up slowly, use for 6 weeks before maximal effect is seen
If Tx fails - refer to specialist urological assessment & management

Surgery may also be considered - tension free vaginal tape (SUI) , colposuspension ( gold standard)

Intermittent catheterisation

Anti andorgens - BPH

20
Q

What is the definition of a fall?

A

An event that results in a person non-intentionally coming to rest at a lower level ( usually the floor).

21
Q

What intrinsic factors (i.e. related to the body directly) are considered causes of falls?

A

Intrinsic:

1) Cardiovascular
-Postural hypotension
-Syncope
-Arrhythmia

2) Neurological & Balance
-Neurological conditions e.g. parkinsons
-Stroke
-Peripheral neuropathy
- BPPV - benign paroxysmal positional vertigo , vestibular disorders e.g. vestibular neuronitis, Meniere’s syndrome

3) Disability (movement / ability)
- Arthritis
-Visual impairment - cataracts, glaucoma, macular degeneration
-Muscle weakness - sarcopenia
- Diabetic foot

22
Q

What extrinsic factors are associated with falls?

A

Extrinsic:

Poly pharmacy - psychiatric medications & cardiovascular, thiazides etc.
Intoxication
Environmental based -lighting, flooring
Foot wear
Bifocal or varifocal glasses

23
Q

What investigations should be considered following a fall?

A

Investigations to look for causes:
- ECG - 24h monitoring if appropriate
- Echocardiogram ( if appropriate)
- CT Head
- Bloods - e.g. FBC, B12, folate, U&Es
- Glucose levels - BMs ( hypo/hyperglycaemia)
- Calcium & phosphate levels
- TFTs ( hypothyroidism)

24
Q

What are the most common complications ( outcomes ) of falling in the elderly?

A

Fractures
Anxiety / lack of confidence
Head injury
Bleeding/ Bruising
Loss of mobility

In long lie - can lead to dehydration, hypothermia, pressure sores & pneumonia, in severe cases of long lie, it can lead to an AKI ( pre renal) and rhabdomyolysis

25
Q

What classes of drugs are associated with precipitating falls in the elderly? (10)

A

Antihypertensives - especially alpha blockers & ACEi
Thiazide diuretics
Antipsychotics
Anticholinergics
Antiarrhythmics
Anticonvulsants
Hypoglycaemics
Opiates
Sedatives - benzodiazepines

26
Q

What is the “get up & go” test ?

A

Simple screening test for gait & balance abnormalities
Patient is asked to rise from a chair without using their arms, walk 3 m then return and sit down in their chair

27
Q

What interventions are in place to reduce falls?

A

** Reducing fall frequency**
1) Drug reviews - reduce polypharmacy / remove drugs that precipitate falls

2) Strength & balance training

3) Walking aids

4) Environmental assessment - Occupational therapy

5) Treat underlying cause

Preventing adverse effects of falls

1) Supervision - starting a POC

2) Teaching patients to get up after falling over - Physio

3) Change of Accommodation - e.g. move to care home or bungalow

4) Lifelines / alarms

28
Q

What is delirium?

A

Syndrome of disturbance of consciousness accompanied by change in cognition not accounted for by a pre-existing condition (e.g dementia, depression, psychotic disorders )

29
Q

What are the key features of delirium? (3)

A

1) Disturbance of consciousness
- decreased clarity of awareness of the environment
- hypoactive, hyperactive or mixed
- decreased ability to focus, shift or sustain attention

2) Change in cognition
- often widespread e.g. memory impairment, disorientation ( time, place, person)
- language disturbance - dysgraphia & dysnosmia
- perceptual impairment - e.g. door slam = gun shot
- illusions & hallucinations

3) Acute onset & fluctuates
- onset over several hours / days
- severity varies throughout day

30
Q

What are the signs of delirium? (DELIRIUM)

A

Disordered thinking
Euphoric, fearful, depressed, angry
Language impaired
Illusions/ delusions/ Hallucinations
Reversal of awake-sleep cycle
Inattention
Unaware/ disorientated
Memory deficits

31
Q

What are the common causes of delirium? (THINK DELIRIUM)

A

THINK DELIRIUM -

Trauma (pain)
Hypoxia
Increasing age/ frailty
NOF fracture
smoKer or alcohol withdrawal

Drugs - new, stopped/started, side effects & drug interactions
Environment - especially ward moves
Lack of sleep - reversal of sleep-wake cycle
Imbalanced electrolytes
Retention - urinary or constipation
Infection/ sepsis
Uncontrolled pain
Medical conditions

32
Q

How do you treat a patient with delirium?

A

Treat underlying cause
Reassure / re orientate
Familiar people / objects
1:1 nursing
Sedate only if distressing symptoms & at significant risk to self or others ( will need a Deprivation of Liberty Safeguarding form completed)

33
Q

What is dementia?

A

Dementia is an acquired, global and progressive cognitive impairment involving one or more cognitive function. E.g.:

  • memory
  • concentration
  • language
  • learning
  • executive function
  • social cognition
34
Q

What are the different types of dementia?

A

Alzheimer’s Disease

Vascular dementia

Lewy body dementia

Frontotemporal dementia (aka Picks disease)

35
Q

What are the basic pathophysiologies of the different types of dementia?

A

**Alzheimer’s Disease **
-caused by formation of beta amyloid plaques & neurofibrillary tangle formation - leads to impaired neuronal signalling & neuronal apoptosis – specifically in cortex

**Vascular dementia **
- Atherosclerosis in carotid arteries/ vertebral arteries supplying brain
- gradual decrease in blood flow —> chronic ischaemia
- plaques can break off & block smaller arteries —> complete lack of blood supply to areas of the brain —> blood supply falls below demands of tissue —> Ischaemic stroke – permanent damage to brain tissue, tissue damaged undergoes Liquefactive necrosis
-Loss of mental functions governed by that area —> dementia, persistent loss of cognitive function

**Lewy body dementia **
- Alpha-synuclein protein —> misfolded within neurones —> aggregates to form Lewy bodies inside neurones ( particularly in cortex & substantia nigra – cholinergic and dopaminergic neurones )

Frontotemporal dementia (aka Picks disease)
- caused by formation of tangled Tau proteins - aka Picks bodies
- genetic cause
-leads to severe atrophy, neuronal loss, gliosis, and presence of abnormal neurons (Pick cells) containing inclusions (Pick bodies)

36
Q

How are some less common causes of dementia?

A

Low thiamine ( alcohol)
Syphilis
Parkinson’s
Normal hydrocephalus
Pellagra
Repeated head trauma
Whipples disease
Huntington’s
CJD

37
Q

What investigations should be considered in diagnosing dementia ?

A

**Cognitive assessment **

MMSE mental state examination
10 minute test, more sensitive than AMT

MoCA – Montreal Cognitive Assessment
most accurate tool – 30 question test, tests:

-Language abilities
-Abstraction
-Attention
-Orientation
-Short term memory
-Executive function
-Calculations
- Visuoconstructional skills

*AMT (abbreviated mental test) *
Scored out of 10, score of seven or under —> query cognitive function

Investigations
To rule out reversible causes ( very uncommon) but should be detected

Bloods
- FBC
-ESR
- B12
- Folate
- U+E
- LFTs
-TSH
-CRP
-syphilis & HIV if there are atypical features

Neuroimaging
-indicated if suspecting early onset dementia
- usually CT

38
Q

How do patients with dementia generally present?

A

Alzheimer’s Disease
- Insidious onset, over many years
- early profound short term memory loss, progresses to broad & global cognitive dysfunction
-behavior problems are common

Vascular Dementia
- Cognitve impairment is more irregular in comparison to AD
- onset is associated with cerebrovascular damage (e.g.stroke)
-deterioration is therefore abrupt & stepwise
- urinary incontinence and falls are early signs

Lewy body dementia
- gradually progressive background dementia, insidious onset
- shorter term fluctuations in cognitive function
- prominent visual & auditory hallucinations with paranoia & delusions

Frontotemporal dementia ( aka picks disease)
- onset is often very early (35-75)
- behavioural and langauge difficulties dominates - disinhibition, mental rigidity
-MMSE does not test frontal lobe - normal cognitive function

39
Q

How is dementia managed?

A

Lifestyle
- encourage physical, mental & social activities
- Occupational therapy - create safe environment at home
- POC in place to aid with daily tasks
- support caregivers - refer to support groups
- educate patients family

Practical
- simplify medications
- suggest memory aids ( lists etc)
- educate and support patient regarding legal and ethical issues ( wills, LPA etc)

Medications

  • AChesterase inhibitors – donepezil, rivastigmine, galantamine) – modest efficacy mild to moderate AD, can slow progression increases ACh levels —> increases neurotransmission
  • NMDA antagonists – Memantine, useful for treating agitation & advanced dementia
  • Benzodiazepines in very anxious/ agitates patients
  • SSRIs in depression